Cardiac Electrophysiology Unit, Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, India.
Circ Arrhythm Electrophysiol. 2019 Aug;12(8):e007387. doi: 10.1161/CIRCEP.119.007387. Epub 2019 Jul 26.
Incessant focal atrial tachycardia (FAT), if untreated, can lead to ventricular dysfunction and heart failure (tachycardia-induced cardiomyopathy). Drug therapy of FAT is often difficult and ineffective. The efficacy of ivabradine has not been systematically evaluated in the treatment of FAT.
The study group consisted of patients with incessant FAT (lasting >24 hours) and structurally normal hearts. Patients with ventricular dysfunction as a consequence of FAT were not excluded. All antiarrhythmic drugs were discontinued at least 5 half-lives before the initiation of ivabradine. Oral ivabradine (adults, 10 mg twice 12 hours apart; pediatric patients: 0.28 mg/kg in 2 divided doses) was initiated in the intensive care unit under continuous electrocardiographic monitoring. A positive response was defined as the termination of tachycardia with the restoration of sinus rhythm or suppression of the tachycardia to <100 beats per minute without termination within 12 hours of initiating ivabradine.
Twenty-eight patients (mean age, 34.6±21.5 years; women, 60.7%) were included in the study. The most common symptom was palpitation (85.7%) followed by shortness of breath (25%). The mean atrial rate during tachycardia was 170±21 beats per minute, and the mean left ventricular ejection fraction was 54.7±14.3%. Overall, 18 (64.3%) patients responded within 6 hours of the first dose of ivabradine. Thirteen of 18 ivabradine responders subsequently underwent successful catheter ablation. FAT originating in the atrial appendages was a predictor of ivabradine response compared with those arising from other atrial sites (P=0.046).
Ivabradine-sensitive atrial tachycardia constitutes 64% of incessant FAT in patients without structural heart disease. Incessant FAT originating in the atrial appendages is more likely to respond to ivabradine than that arising from other atrial sites. Our findings implicate the funny current in the pathogenesis of FAT.
持续性局灶性房性心动过速(FAT)如果不治疗,可导致心室功能障碍和心力衰竭(心动过速性心肌病)。药物治疗 FAT 往往困难且无效。伊伐布雷定在治疗 FAT 中的疗效尚未得到系统评估。
研究组由持续性 FAT(持续时间>24 小时)且心脏结构正常的患者组成。不排除因 FAT 导致心室功能障碍的患者。在开始使用伊伐布雷定之前,所有抗心律失常药物均至少停药 5 个半衰期。在持续心电图监测下,口服伊伐布雷定(成人,10 mg,每 12 小时 2 次;儿科患者:0.28 mg/kg,分 2 次服用)在重症监护病房开始。阳性反应定义为心动过速终止,窦性心律恢复或心动过速抑制至<100 次/分钟,但在开始伊伐布雷定后 12 小时内未终止。
28 例患者(平均年龄 34.6±21.5 岁;女性占 60.7%)纳入研究。最常见的症状是心悸(85.7%),其次是呼吸急促(25%)。心动过速时的平均心房率为 170±21 次/分钟,平均左心室射血分数为 54.7±14.3%。总体而言,18 例(64.3%)患者在伊伐布雷定首剂后 6 小时内出现反应。18 例伊伐布雷定反应者中有 13 例随后成功接受导管消融。与起源于其他心房部位的 FAT 相比,起源于心房附件的 FAT 是伊伐布雷定反应的预测因素(P=0.046)。
无结构性心脏病患者持续性 FAT 中,伊伐布雷定敏感的房性心动过速占 64%。起源于心房附件的持续性 FAT 比起源于其他心房部位的 FAT 更有可能对伊伐布雷定产生反应。我们的发现提示有趣电流在 FAT 的发病机制中起作用。